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Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger
Author(s) -
Shembalkar Prafulla K.,
Till Silke,
Boettger Michael K.,
Terenghi Giorgio,
Tate Simon,
Bountra Chas,
Anand Praveen
Publication year - 2001
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1053/eujp.2001.0251
Subject(s) - glial cell line derived neurotrophic factor , nerve growth factor , neurotrophic factors , neurotrophin , inflammation , immunohistochemistry , nociception , medicine , neuroscience , psychology , receptor
The sodium channels SNS/PN3 and NaN/SNS2 are regulated by the neurotrophic factors—nerve growth factor (NGF) and glial‐derived neurotrophic factor (GDNF), and may play an important role in the development of pain after nerve injury or inflammation. These key molecules have been studied in an amputated causalgic finger and control tissues by immunohistochemistry. There was a marked increase in the number and intensity of SNS/PN3‐immunoreactive nerve terminals in the affected finger, while GDNF‐immunoreactivity was not observed, in contrast to controls. No differences were observed for NGF, trk A, NT‐3 or NaN/SNS2‐immunoreactivity. While further studies are required, these findings suggest that accumulation of SNS/PN3 and/or loss of GDNF may contribute to pain in causalgia, and that selective blockers of SNS/PN3 and/or rhGDNF may provide effective novel treatments.